Endothelial Progenitor Cell Response to Acute Multicomponent Exercise Sessions with Different Durations

Simple Summary Reports suggest that an acute bout of exercise promotes the mobilization of endothelial progenitor cells from bone marrow, increasing the circulating levels of endothelial progenitor cells. The impact of the intensity of acute exercise on the circulating levels of endothelial progenitor cells was previously described. Yet, the question of whether the duration of the exercise session impacts the mobilization of endothelial progenitor cells has not been tested among adults with cardiovascular risk factors. In this study, a 30 min session vs. a 45 min session promoted a significant increase in the circulating number of endothelial progenitor cells. The findings show a multicomponent exercise session of only 30 min has the potential to induce beneficial effects for vascular health. It is widely accepted that exercise training has beneficial effects on vascular health. Although a dose-dependent relation has been suggested, little is known about the effects of different exercise durations on endothelial markers. This study aimed to assess the effect of single exercise sessions with different durations in the circulating levels of endothelial progenitor cells (EPCs) and endothelial cells (CECs) among adults with cardiovascular risk factors. Ten participants performed two multicomponent exercise sessions, one week apart, lasting 30 and 45 min (main exercise phase). Before and after each exercise session, blood samples were collected to quantify EPCs and CECs by flow cytometry. The change in EPCs was significantly different between sessions by 3.0% (95% CI: 1.3 to 4.7), being increased by 1.8 +/- 1.7% (p = 0.009) in the 30 min session vs. -1.2 +/- 2.0% (p > 0.05) in the 45 min session. No significant change was observed in CECs [-2.0%, 95%CI: (-4.1 to 0.2)] between the sessions. In conclusion, a multicomponent exercise session of 30 min promotes an acute increase in the circulating levels of EPCs without increasing endothelial damage (measured by the levels of CECs) among adults with cardiovascular risk factors.